Regression Of Vascular Calcification Research Articles

Role of Macrophages in the Progression and Regression of Vascular Calcification.

Vascular calcification is an abnormal cell-mediated process in which bone-specific hydroxyapatite crystals are actively deposited on the blood vessel wall and is a significant pathological basis for the increased incidence and mortality of adverse cardiovascular events. Macrophages play an important regulatory role in the occurrence, development, and regression of vascular calcification. After the tissue microenvironment changes, macrophages subsequently change their polarity and phenotype or secrete functional substances as an adaptive response. As research on macrophages continue to move into this field, we gain a new understanding of the mechanism of the formation and regression of vascular calcification, which might offer valuable new intervention targets for the prevention and inhibition of vascular calcification. This review summarizes a wealth of research in this field and explores the roles of macrophages in the development process of vascular calcification.

Regression of vascular calcification in a parathyroidectomized patient on dialysis with untreated hypocalcemia over 12-year follow-up

Although some experimental targets involved in calcium deposition are emerging, no intervention has been described to reliably reverse vascular calcification (VC). We report a case of severe VC regression in a parathyroidectomized patient on hemodialysis over 12-year follow-up, highlighting the use of calcium-free phosphate binders and a 2.5 mEq/L calcium dialysate for reducing calcium loading, despite persistent asymptomatic hypocalcemia occurrences. This case suggests that phosphate-binder choice and calcium dialysate concentration could be influenced by other components of CKD-MBD besides biochemical parameters, such as the presence of VC, so concluding that asymptomatic hypocalcemia may not be as harmful as once supposed, and conferring greater prognostic weight to the presence of VC than to calcium levels. .

Regression of vascular calcification in chronic kidney disease – feasible or fantasy? A review of the clinical evidence

The complex relationships between cardiovascular, renal, and bone disease are increasingly recognized but not yet clearly understood. Vascular calcification (VC) represents a common end point between these interlinked systems. It is highly prevalent in chronic kidney disease (CKD) and may be responsible for some of the excess cardiovascular events seen in this condition. There is much interest in developing therapeutic agents to stop its development or reverse its progression. Traditionally considered to be due to abnormalities in calcium and phosphate metabolism alone, VC is now known to be the product of active, dynamic processes within the vessel wall. Primary prevention of VC is possible through successful prevention or reversal of progressive renal dysfunction, hypertension and hyperlipidaemia, but is challenging given the increasing global prevalence of these risk factors. Secondary prevention of VC through tight control of calcium and phosphate, can be achieved by dietary or pharmacological means. Both the modification of haemodialysis duration or methods and the use of renal transplantation have an effect. Novel drugs such as cinacalcet were hoped to halt calcification but results have been mixed, and no intervention has yet been shown to reverse calcification reliably. A new range of experimental targets involved in the putative mediatory pathways between bone and vascular disease has emerged. Aiming to manipulate the active mechanisms involved in calcium deposition, these hold hope for reversal of calcification, but are still theoretical or in early animal or human experimentation.

Regression of vascular calcification in a patient treated with cinacalcet: a case report.

The purpose of this case report is to describe the regression of vascular calcifications (VC) in a patient with secondary hyperparathyroidism (SHPT) after having added cinacalcet to her treatment. We present the clinical case of a 48-year-old woman with chronic renal failure secondary to tubulointerstitial disease. She was being treated with long-term haemodialysis (HD) and underwent two kidney transplants with transplantectomies. The patient presented with severe SHPT caused by parathyroid gland hypertrophy. The radiology test showed signs of VC in the radial and interdigital arteries, and VC in a linear arrangement were observed in both breasts on the mammography. Cinacalcet was added to her treatment with vitamin D derivatives and phosphate-binding agents, which resulted in a good control of mineral metabolism. The radiology test showed that the calcification in the interdigital artery had disappeared and that the bone appeared to be more structured. The mammography also showed regression of the VC. To conclude, cinacalcet may have potential for regression of VC in patients with SHPT.

The pathophysiology of vascular calcification: are osteoclast-like cells the missing link?

There is increasing evidence to suggest that the initiation of vascular calcification is an active process involving vascular smooth muscle cell (VSMC) apoptosis and trans-differentiation into calcifying cells. This active process results in the deposition of an osteogenic extracellular matrix and may be exacerbated by a reduction in the levels of one or more native calcification inhibitors (such as fetuin A and pyrophosphate). Here, we present data which strongly suggest that the regression of vascular calcification might also be an active cellular process involving osteoclast-like cells. However, the presence of osteoclast like cells in the vascular wall is rather limited. To explain this rarity of osteoclast-like cells, we recently observed that the same factors, which promote the trans-differentiation of VSMCs into osteoblastlike cells are also capable of inhibiting the in vitro differentiation of monocytes/macrophages into osteoclast-like cells. An imbalance between osteoblast-like and osteoclast-like cell activities would therefore favour the occurrence of a pathological calcification process in vessel walls. Our new data are strongly evocative of a vascular remodelling process similar to that observed in bone tissue. To confirm this hypothesis, strategies for activating osteoclasts in the vascular wall (with a view to preventing or reversing vascular calcifications) are required.